How Do Computational Models of the Role of Dopamine as a Reward Prediction (original) (raw)
Related papers
2006
How Do Computational Models of the Role of Dopamine as a Reward Prediction Error Map on to Current Dopamine Theories of Schizophrenia? Angela J. Thurnham* (a.j.thurnham@herts.ac.uk), D. John Done** (d.j.done@herts.ac.uk), Neil Davey* (n.davey@herts.ac.uk), Ray J. Frank* (r.j.frank@herts.ac.uk) School of Computer Science,* School of Psychology, **University of Hertfordshire, College Lane, Hatfield, Hertfordshire. AL10 9AB United Kingdom reward prediction, or TD error, including evidence that the RPE model of dopamine activity applies to humans as well as primates. The biological plausibility of existing neural network models by Cohen & Servan-Schreiber, (1992); Braver Barch & Cohen, (1999); Suri & Schultz, (1999); Rougier, Noelle, Braver, Cohen & O’Reilly, (2005) and O’Reilly & Frank, (2006) are then discussed in the light of the afore-mentioned dopamine theories of schizophrenia. Finally, we conclude with four major questions arising from recent dopamine theories of schizophrenia th...
Frontiers in psychiatry, 2013
Abnormalities in reinforcement learning are a key finding in schizophrenia and have been proposed to be linked to elevated levels of dopamine neurotransmission. Behavioral deficits in reinforcement learning and their neural correlates may contribute to the formation of clinical characteristics of schizophrenia. The ability to form predictions about future outcomes is fundamental for environmental interactions and depends on neuronal teaching signals, like reward prediction errors. While aberrant prediction errors, that encode non-salient events as surprising, have been proposed to contribute to the formation of positive symptoms, a failure to build neural representations of decision values may result in negative symptoms. Here, we review behavioral and neuroimaging research in schizophrenia and focus on studies that implemented reinforcement learning models. In addition, we discuss studies that combined reinforcement learning with measures of dopamine. Thereby, we suggest how reinfo...
Theoretical Research Proposal - Against the dopamine hypothesis of schizophrenia.
2013
1950's -Origin of Dopamine Hypothesis. First antipsychotics used to treat schizophrenia. Called "typical" antipsychotics or major tranquilizers. Inverse agonist on D 1 -D 5 . Frequently induce debilitating side-effects in the Extrapyramidal System. 1970's -Atypical antipsychotics introduced. Second generation antipsychotics, dopamine and serotonin receptor antagonists. Considered to have fewer side-effects. 1991 -Dopamine Hypothesis version II. Davis et al. Dopamine in Schizophrenia: A Review and Reconceptualization. Mid-late 2000's-Genomics revolution takes off in neuropsychiatry. Cheaper and more robust genomic technologies provide hundreds of candidate loci/molecules associated with schizophrenia. 2007 -First mouse model of schizophrenia developed. First model based on genetic manipulation. Future models would include manipulations to DISC1, NRG1, Dysbindin, Calcinuerin, and Reelin. 2009 -The Dopamine Hypothesis of Schizophrenia: Version III. The Final Common Pathway. Howes O. and Kapur S. 2012 -"Golden age" of CBT in treatment of schizophrenia. Increased success in the used of CBT for treatment of schizophrenia emphasizes the involvement of neuroplasticity in disease progression and treatment. 2013 -A serotonin hypothesis of schizophrenia. Review published by A. E. Eggers in Medical Hypotheses.
Dopaminergic mechanisms and cognitive deficit in schizophrenia
Psychopharmacology, 1979
A hypothesis is briefly discussed proposing that schizophrenic symptoms are due to a breakdown in a mechanism by which conscious attention is limited and directed. It is shown that this mechanism can be modelled in terms of a simple nerve network in which every channel infiibits all the others. Failure of this inhibition would cause the defect hypothesised to occur in schizophrenia.
The Lancet, 1976
The antipsychotic actions and extrapyramidal side-effects of neuroleptic drugs are strongly correlated with their ability to block central dopaminergic transmission. It is argued that the former are more closely related to actions on dopaminergic mechanisms in the "mesolimbic dopamine" system, and the latter to similar actions in the striatum. Although the amphetamine psychosis closely resembles paranoid schizophrenia and may be due to excess dopamine release, clinical, biochemical, and endocrine studies suggest that dopaminergic overactivity is not a necessary concomitant of schizophrenic illnesses. It is suggested that the primary defect in schizophrenia does not lie in the dopamine neuron. It remains to be excluded that the receptors, particularly in the mesolimbic dopamine areas, become supersensitive, or that there is a deficit in a system which normally acts in antagonism to the mesolimbic dopamine system.
Hippocampal dysregulation of dopamine system function and the pathophysiology of schizophrenia
Trends in Pharmacological Sciences, 2011
Substantial evidence suggests that psychosis in schizophrenia is associated with a dysregulation of subcortical dopamine system function. Here we examine evidence that this dysregulation is secondary to hyperactivity within hippocampal subfields. Enhanced hippocampal activity has been reported in both preclinical models and in schizophrenia patients. Moreover, this hippocampal hyperactivity is correlated with enhanced dopamine neuron activity and positive symptoms, respectively. Thus, restoration of hippocampal function could provide a more effective therapeutic approach than current therapeutics based on dopamine D2 receptor blockade. Indeed, initial studies demonstrate that allosteric modulation of the α5GABA A receptor can decrease aberrant dopamine signaling and associated behaviors in a verified rodent model of psychosis.
Dopamine Hypothesis of Schizophrenia Revisited
Psychiatric Annals, 1993
- The effects of antipsychotic agents in blocking dopamine (DA) receptors and the similarity between paranoid schizophrenia and amphetamine-induced psychosis have opened new research areas in schizophrenia. (2) This paper reviews studies on the hypothesized role for DA in schizophrenia, specifically defects in the DA system including receptor supersensitivity and other dysfunctions. While clinical studies seem to support the DA hypothesis, evidence from the evaluation of spinal fluid homovanillic acid (HVA), dopamine~13-hydroxylasc (DBH) and plasma prolactin has been inconclusive. (4) Schizophrenic symptoms fluctuate with central DA activity and some positive brain autopsies appear to support the notion of dysfunctional DA systems. (5) Increasing evidence suggests that other neurotransmitters or modulators of DA activity, such as amino acids (e.g. GABA), amines (norepinephrine) or peptides (endorphins), may be involved in the regulation of psychosis. The author suggests that more specific presynaptic DA agonists and agents that specifically affect mesolimbic DA systems should be developed to test the DA hypothesis further. The mechanism of hgw DA activity affects schizophrenia has not yet been elucidated.